HIV Flashcards

1
Q

What cells do HIV hijack?

A

T-helper cells

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2
Q

Describe briefly the pathogenesis of HIV infection

A

1: HIV binds T helper cell with it’s gp120 binding to T helper cells CD4
2: viral envelope fuses with t helper cell membrane and viral RNA enters cell
3: viral reverse transcriptase manufactures DNA from RNA
4: viral integrase integrates DNA to host DNA
5: viral DNA transcribed/translated = viral proteins
6: new virus assembled and bud out of T helper cell = t helper cell death
- infected t cells also killed by t killer cells

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3
Q

Describe the phases of HIV infection

A

1: infection
- infection mucosal CD4 cell, transport to regional lymph nodes, established infection within 3 days, dissemination virus

2: acute phase
- HIV Abs +ve in blood 3-12 wks
- within 2-4wks flu-like symptoms 80%/macular-papular upper body rash
- rapid replication virus and loss t helper cells
- v high risk transmission
- after few weeks T killer cells destroy t helpers and greatly reduce rate viral replication

3: asymptomatic infection
- prolonged phase (may last years)
- virus continues to replicate rapidly but no. kept in check by immune system
- may be no symptoms but increased tendency to suffer colds/infection that are slow to go away
- dormant diseases e.g shingles/TB reactivate

4: disease phase (AIDS)
- decreased no. of t helper cells and increased viral load
- opportunistic infections
- weight loss
- dementia
- kaposi sarcoma

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4
Q

What is an opportunistic infection?

A

-pathogen that doesn’t normally cause a disease in a healthy person

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5
Q

Pneumocystitis pneumonia = opportunistic infection

  • what organism causes this?
  • what CD4 threshold does this increase the risk for?
  • what signs/symptoms are seen
  • CXR
  • how is this diagnosed?
  • treatment?
  • what prophylaxis for this exists?
A

Organisms:
-pneumocystitis jiroveci: most common infection seen/diffuse infection

CD4 threshold: <200

Symptoms: insidious onset/dry cough/SOB

Signs: exercise desaturation - ask patient to do exercise and see SOB

CXR: may be normal, interstitial infiltrates, reticulonodular markings

Diagnosis: BAL + immunofluorescence +/- PCR

Treatment: high does co-trimoxazole (+/- steroid)

prophylaxis: low dose co-trimoxazole

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6
Q

What kind of TB infection is more commonly seen in HIV patients?

A
  • symptomatic primary infection/reactivation latent
  • lymphodenopathy
  • miliary TB
  • extra-pulmonary TB
  • multi-drug resistant TB
  • immune reconstitution syndrome
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7
Q

Cerebral toxoplasmosis is an opportunistic infection that affects HIV patients:

  • organism?
  • CD4 threshold?
  • what does this cause?
  • signs and symptoms?
A

Organism: toxoplasma gondii

CD4: <150

Clinical features: reactivation latent infection/multiple cerebral abscesses

S/S: headache/fever/focal neurology/siezures/decreased conscious level/raised ICP

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8
Q

Cytomegalovirus is an opportunistic infection that affects HIV patients:

  • CD4 threshold
  • what does this cause?
  • signs/symptoms
  • what screening is done?
A

CD4 < 50 (late stage), reactivation of latent infection

can cause: retinitis, colitis, oesophagitis

S/S: decreased visual acuity, floaters, abdo pain, diarrhoea, PR bleeding

Screening: ophthalmic screening for all individuals <50 CD4

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9
Q

What skin infections are seen in HIV patients?

A

Herpes zoster - multidermatomal and recurrent

Herpes simplex - extensive, hypertrophic, acyclovir resistant

HPV - extensive, recalcitrant, dysplastic

(also penicilliosis/histoplasmosis)

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10
Q

What neurological presentations can HIV cause?

A
  • HIV assoc. cognitive impairment
  • progressive multifocal neuroencephalopathy
  • distal sensory polyneuropathy
  • mononeuritis multiplex
  • vacuolar myelopathy
  • aseptic meningitis
  • G-B syndrome
  • viral meningitis
  • cryptococcal meningitis
  • neurosyphillis
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11
Q

What is HIV assoc. cognitive impairment?

A

-reduced short term memory with motor dysfunction

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12
Q

progressive multifocal neuroencephalopathy:

  • what organism causes this?
  • what s/s seen?
A

Organism: JC virus/reactivation latent virus

S/S: rapidly progressive, focal neurology, confusion, personality change

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13
Q

What is slim’s disease? what are the causes?

A

HIV assoc. wasting

  • metabolic (chronic immune activation)
  • GALT is wiped out
  • anorexia
  • diarrhoea
  • malabsorption
  • hypogonadism
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14
Q

What cancer is assoc. with HIV? what is this caused by? what is this treated with?

A

Kaposi sarcoma: vascular tumour
Non-hogkins lymphoma
cervical cancer

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15
Q

Kaposi sarcoma:

what is this caused by? what is this treated with?

A

-HPV

Treatment: HAART/local therapies/systemic chemo

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16
Q

Non-hodgkins lymphoma in HIV:

  • symptoms
  • diagnosis
  • treatment
A

Symptoms:
-more advanced/B symptoms/bone marrow involvement/extranodal disease/ increased CNS involvement

Diagnosis - as for HIV

Treatment- HAART

17
Q

Cervical cancer in HIV:

-prevention?

A

All complicated HPV disease = offer HIV test

Smears given yearly for HIV pt.s

18
Q

What other non-opportunistic infections can be seen in HIV?

A
  • mucosal candidiasis
  • seborrheic dermatitis
  • diarrhoea
  • fatigue
  • worsening psoriasis
  • lymphadenopathy
  • parotitis
  • STIs/Hep C/Hep B
19
Q

How is HIV transmitted?

A

Sex (most common mode in UK):

  • anoreceptive
  • trauma
  • genital ulceration
  • concurrent STI

Mother to child transmission:

  • in-utero
  • transplacental
  • delivery
  • breast feeding

Parenteral:

  • injecting drugs use
  • infected blood products
  • iatrogenic
20
Q

with regards to HIV testing, in which clinical settings are ‘opt out’? why is this?

A

Higher prevalence HIV in people accessing these services:

  • termination of pregnancy services
  • GUM clinic
  • drug dependancy clinics

Risk assoc. with undiagnosed is too high:

  • antenatal services
  • assisted conception services
21
Q

With regards to screening ‘high risk groups’: who are these?

A

Prevalence higher HIV than in background population/regular screening recommended:

  • MSM
  • Female partners MSM
  • IVDU
  • Partners HIV+ pts

Subsaharan africa/Carribean/Thailand, regular screening recommended:

  • Adults from endemic areas
  • Children from endemic areas
  • Sexual partners from endemic areas
  • Hx of iatrogenic exposure in endemic areas
22
Q

What is the treatment for HIV?

A

Highly active antiretroviral therapy

-combination of 3 drugs from at least 2 drug classes

23
Q

What are the adverse effects of HAART?

A

GI effects and transaminitis, fulminant hepatitis

skin: rash, hypersensitivity, stevens-johnson

CNS: mood/psychosis

Renal: proximal renal tubulopathies

Bone: osteomalacia

CVS: increased MI risk

Haem: anaemia

24
Q

Which drugs are liver enzyme inhibitors?

A

Protease inhibitors and non-nucleoside reverse transcriptase inhibitors

25
Q

What precautions are taken for HIV +ve male and HIV -ve female who are trying to concieve?

A
  • Sperm washing with IUI/IVF

- timely UPSI with HAART +/- pre-exposure prophylaxis

26
Q

What precautions are taken for HIV-ve male and HIV=ve female who are trying to concieve?

A
  • self insemination

- timely UPSI with HAART

27
Q

Can a HIV+ve female have vaginal delivery?

A

YES if HAART throughout pregnancy and there is undetected viral load, if detected do C-section

28
Q

What precautions are taken after a HIV+ve female has given birth?

A
  • Baby = Post exposure prophylaxis for 4mths

- Exclusively formula fed

29
Q

What HIV testing is available?

A

RNA - first to be detected and detected in babies
Ab test - shows chronic HIV
(antigen test +ve and Ab -ve = new infection)